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Decrease in inflammatory hyperalgesia by herpes vector-mediated knockdown of Nav1.7 sodium channels in primary

D C Yeomans1, S R Levinson, M C Peters

  • 1Department of Anesthesia and Stanford Pain and Analgesia Research Center, Stanford University, Stanford, CA 94305-5117, USA. dcyeomans@stanford.edu

Human Gene Therapy
|March 12, 2005
PubMed
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Peripheral inflammation increases Nav1.7 sodium channel expression, leading to hyperalgesia. Blocking Nav1.7 expression with an antisense vector prevented this increase and reduced pain sensitivity.

Area of Science:

  • Neuroscience
  • Pain Research
  • Molecular Biology

Background:

  • Peripheral inflammation elevates Nav1.7 sodium channel expression in sensory neurons, potentially enhancing neuronal excitability.
  • Inflammation-induced hyperalgesia in humans and increased nociceptive responsiveness in animals are observed phenomena.

Purpose of the Study:

  • To investigate the direct relationship between increased Nav1.7 sodium channel expression and the development of inflammatory hyperalgesia.
  • To determine if inhibiting Nav1.7 expression can prevent inflammation-induced pain sensitization.

Main Methods:

  • A recombinant herpes simplex virus vector encoding an antisense sequence to Nav1.7 and GFP was applied to mouse hindpaw skin.
  • Complete Freund's adjuvant was used to induce peripheral inflammation in the hindpaws.

Related Experiment Videos

  • Nav1.7 expression levels and thermonociceptive responses (C and Adelta fibers) were assessed in GFP-positive neurons.

    • Main Results:

    • The Nav1.7 antisense vector successfully prevented the upregulation of Nav1.7 expression in sensory neurons following inflammation.
    • Mice treated with the Nav1.7 antisense vector did not develop hyperalgesia in response to inflammatory stimuli.
    • Control vector treatment (GFP only) did not affect Nav1.7 expression or hyperalgesia development.

    Conclusions:

    • Increased Nav1.7 sodium channel expression in nociceptive neurons is a key contributor to inflammatory hyperalgesia.
    • Targeting Nav1.7 expression presents a potential therapeutic strategy for managing inflammatory pain.